Light-emitting diode-derived blue light overexposure accelerates corneal endothelial cell aging by inducing abnormal...

Area of Science:

• Ophthalmology
• Cell Biology
• Biochemistry

Background:

• Blue light, a high-energy portion of the visible spectrum (400-500 nm), is increasingly prevalent due to widespread LED use.
• Corneal endothelial cells (CECs) are vital for maintaining corneal transparency and clear vision.
• The impact of blue light on CECs and corneal endothelium aging is not well understood.

Purpose of the Study:

• To investigate the effects of blue light irradiation on corneal endothelial cells (CECs).
• To elucidate the mechanisms underlying blue light-induced corneal endothelium aging.

Main Methods:

• Established in vivo and in vitro models of light-emitting diode (LED) blue light irradiation.
• Examined CEC fate, including senescence, dysfunction, and apoptosis.
• Assessed indicators of oxidative stress, focusing on reactive oxygen species (ROS) and mitochondrial function.
• Investigated the role of the Nrf2 signaling pathway.

Main Results:

• Blue light exposure significantly increased ROS production in CECs, leading to mitochondrial oxidative stress.
• This oxidative stress induced CEC senescence, dysfunction, and apoptosis, accelerating corneal endothelium aging and cell loss.
• Early-stage ROS elevation activated the Nrf2 signaling pathway.
• Nrf2 pathway activation demonstrated protective effects, inhibiting CEC senescence.

Conclusions:

• Blue light exposure contributes to corneal endothelium aging through oxidative stress and subsequent CEC apoptosis.
• The Nrf2 signaling pathway plays a protective role in mitigating blue light-induced damage to CECs.
• Findings provide insights into the mechanisms of blue light-related corneal aging and potential therapeutic targets.